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PubMed1996

[A comparison of bezafibrate and lovastatin treatment at the usual doses in post-heart transplant hyperlipemia].

INTRODUCTION: Coronary artery disease is a major limiting factor for long-term survival after heart transplantation. Hyperlipidemia is a probable risk factor for coronary artery disease in this kind of patient. Bezafibrate and lovastatin have proved to be effective in lowering total and low density lipoprotein cholesterol. The present study tested the safety and efficacy of both drugs on lipid levels in 21 patients with post-heart transplantation hyperlipidemia. PATIENTS AND METHODS: Patients maintained the same diet for three months. Then, they were randomized to lovastatin (20 mg/day) or bezafibrate (400 mg/day) for 8 weeks, and then, crossovered to an additional 8 weeks of bezafibrate or lovastatin. RESULTS: Both drugs were effective in lowering total and low density lipoprotein cholesterol and apoprotein B concentrations, but the effect of lovastatin was significantly greater. Only bezafibrate produced a significant reduction in total triglycerides and a significant rise in high density lipoprotein cholesterol and apoprotein AI. The total cholesterol/high density lipoprotein cholesterol and low density lipoprotein cholesterol/high density lipoprotein cholesterol ratios were decreased under both treatments. CONCLUSION: Both drugs, bezafibrate and lovastatin appear to be safe, effective and well-tolerated therapies for hyperlipidemia in cardiac transplant recipients.

Adult↗
PubMed1998

Results of the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT) and an update on trials now in progress.

Bezafibrate is a latest generation fibrate derivative that substantially reduces total plasma cholesterol and triglyceride concentrations and increases high density lipoprotein (HDL) cholesterol. The Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT) was a double-blind, placebo-controlled trial over 5 years to assess the angiographic benefits of bezafibrate retard (400 mg. day (-1) in young, male, post-myocardial infarction (post-MI) patients. The trial demonstrated that without lowering serum low density lipoprotein cholesterol, progression of coronary atherosclerosis was prevented and the coronary event rate reduced. In subgroup analyse, bezafibrate decreased the rate of progression of coronary atherosclerosis and coronary event rate in young post-MI patients, primarily by slowing the progression of mild-to-moderate lesions. Additional studies are underway to explore further the benefits of this fibrate in coronary heart disease. The Bezafibrate Infarction Prevention study is the first trial to investigate the effects of raising HDL cholesterol and lowering triglycerides in patients with established coronary disease. The Lower Extremity Arterial Disease Event Reduction study is assessing the benefit of lowering fibrinogen in the prevention of major ischaemic heart disease and stroke in patients with peripheral vascular disease.

Adult↗
PubMed1978

The effect of bezafibrate on the fibrinolytic enzyme system and the drug interaction with racemic phenprocoumon.

The influence of a new hypolipidaemic agent, bezafibrate, on anticoagulant requirements and fibrinolysis was studied in 15 patients with hyperlipidaemia on long-term treatment with racemic phenprocoumon. Our results suggest a dose-dependent augmentation of the anticoagulant response to the coumarin drug. Treatment with bezafibrate at 450 and 600 mg daily required a reduction of the phenprocoumon dose by 18.5 and 33.5%, respectively. Correspondingly, the serum level of phenprocoumon decreased by 11.6 and 35.3%. No evidence for an altered drug elimination of racemic phenprocoumon could be found during treatment with bezafibrate. The results support the hypothesis that bezafibrate and analogous hypolipidaemic drugs enhance the response to oral anticoagulant drugs by increasing the affinity of the receptor site for coumarins or the rate of degradation of the vitamin-K-dependent clotting factors. The investigation of the fibrinolytic enzyme system demonstrated an increase of the fibrinolytic activity by enhancing the activity of the plasminogen activator. The lysis time for euglobulin clot was reduced significantly, plasma fibrinogen only moderately. The antiplasmin activity could not be altered substantially by a decrease of alpha1-antitrypsin and a slight increase of alpha2-macroglobulin. In contrast with the inhibition of platelet function the effect of bezafibrate on the fibrinolytic enzyme system showed no dose dependence.

4-Hydroxycoumarins↗
PubMedDate not supplied

Pravastatin compared to bezafibrate in the treatment of dyslipidemia in insulin-treated patients with type 2 diabetes mellitus.

BACKGROUND: Both HMG-CoA reductase inhibitors and fibric acid derivates are used for the treatment of dyslipidemia in Type 2 diabetes patients. The aim of this study was to compare the lipid lowering effect of 40 mg pravastatin, a HMG-CoA reductase inhibitor, and 400 mg bezafibrate, a fibric acid derivate, on serum lipids, lipoproteins and lipoprotein composition in 45 (22 men and 23 women) dyslipidemic, insulin-treated Type 2 diabetes patients. METHOD: The study used a double-blind, cross-over design. RESULTS: Pravastatin treatment was more effective in reducing total cholesterol, LDL-cholesterol, LDL-triglycerides, LDL-ApoB and LDL/HDL-cholesterol ratio (all p<0.001 between groups) and total/HDL-cholesterol and ApoA1/LDL-ApoB ratios (both p<0.01) and always induced a decrease in LDL-cholesterol concentrations and LDL/HDL-cholesterol ratio irrespective of baseline triglyceride concentration. Bezafibrate was more effective in increasing HDL-cholesterol (p<0.01 between groups), ApoA1 lipoprotein and decreasing triglycerides (both p<0.001 between groups) but induced an increase in LDL-cholesterol concentration particularly in patients with baseline triglyceride concentrations exceeding 2.0 mmol/l. With bezafibrate treatment the LDL-cholesterol/LDL-ApoB ratio showed a tendency to rise, suggesting a change in the LDL particle composition to a less small and dense form, while pravastatin treatment induced a decrease in this ratio suggesting a change in the LDL particle to a more dense form. With pravastatin treatment a small rise in HbA(1c) was observed. CONCLUSION: Pravastatin treatment is superior in lowering cholesterol-enriched lipoprotein subpopulations and improving cardiovascular risk factors. Bezafibrate is more effective in raising HDL-cholesterol and alters LDL particle composition to a more favorable form.

Adult↗
PubMed2000

Pharmacodynamic effects of bezafibrate and niacin combination: implications of the mode of administration.

The goal of this investigation was to optimize antilipid therapy by utilizing the combined activity of two lipid-lowering agents, niacin and bezafibrate, and improve their efficacy by targeting them to their presumed presystemic site(s) of action. Thus, continuous duodenal (IGI) administration of the drug combination should augment their efficacy in comparison with intermittent oral treatment. Three hyperlipidemic rat models were studied: Models A and B were based on cholesterol-enriched diets and Model C was based on on acute hyperlipidemia induced by triton injection. Continuous IGI administration of the drug combination [bezafibrate, 30mg/kg/day, and niacin, 40 mg/kg/day for 3 days (Models A and B) or for 18 h (Model C)] produced significantly greater lowering of total cholesterol and triglycerides and elevation of high-density lipoprotein (HDL) cholesterol in comparison with intermittent oral administration of the same doses either given individually or in combination (Models A and B). Similar results were found in Model C for the IGI administration of the drug combination in contrast to oral and also to intravenous infusions. The results indicate that the combination of bezafibrate and niacin produces a significant hypolipidemic response, with major site(s) of action located presystemically. Because a slow-release matrix tablet of the drug combination resulted in a similar magnitude of effect as the IGI administration, the present study provides a pharmacodynamic rationale for the use of a slow-release low-dose niacin-bezafibrate combination.

Animals↗
PubMed1995

High-density lipoprotein and apolipoprotein A-I deficiency induced by combination therapy with probucol and bezafibrate.

The effects of the administration of slow-release bezafibrate to hypercholesterolaemic patients who were already receiving long-term probucol treatment (mean 865 days, 500-1000 mg.day-1) were investigated. Bezafibrate was administered at either 200 mg.day-1 (13 males, 13 females, mean age 55.2 years) or 400 mg.day-1 (11 males, 14 females, mean age 57.2 years), and blood was taken at 0, 3, 6 and 12 months after the beginning of combination therapy. Overall, serum total cholesterol (TC), triglyceride (TG), very low density lipoprotein (VLDL)-TC, high-density lipoprotein (HDL)-TG, VLDL-TG, VLDL-phospholipid (PL), lipoprotein (a) [Lp(a)], apolipoprotein (apo) C-III, apo E levels and LCAT activity decreased significantly with this combination therapy, while HDL cholesterol (C), HDL3-C, HDL-PL, apo A-I and apo A-II levels significantly increased, as assessed by analysis of variance (ANOVA). Five patients (one receiving 200 mg.day-1, four receiving 400 mg.day-1 bezafibrate) showed drastic reductions in HDL-C (HDL-C levels were reduced by a mean of 46.2%, 59.3% and 61.6% at 3, 6 and 12 months, respectively) after beginning combination therapy. These HDL-C reductions were maintained for the 1 year of combination therapy, but then returned to pre-combination treatment levels 1 month after discontinuation of bezafibrate. Serum probucol concentrations and cholesteryl ester transfer protein (CETP) mass were assayed at 6 months, and the probucol concentration was higher in the HDL-deficient group (56.2 vs 26.5 micrograms/ml). In contrast, CETP mass was significantly lower in HDL-deficient patients than in non-HDL-deficient patients (2.08 vs 2.87 mg.1-1)(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Effects of clofibrate, bezafibrate, fenofibrate and probucol on plasma lipolytic enzymes in normolipaemic subjects.

Ten male, normolipaemic, non-obese subjects were given clofibrate 2 g daily, fenofibrate 300 mg daily, bezafibrate 600 mg daily and probucol 1 g daily for eight days, in a crossover study with a wash-out period of 4-8 weeks between each drug regimen. Clofibrate, fenofibrate and bezafibrate caused a significant decrease in serum triglycerides, total cholesterol and LDL-cholesterol concentrations. Probucol caused a significant increase in serum LDL-cholesterol concentration. Serum HDL-cholesterol concentration was significantly increased by bezafibrate and significantly decreased by probucol. All drugs but probucol led to a significant rise in the activity of the plasma lipoprotein lipase; there was not a significant increase in the activity of plasma hepatic lipase after any drug. The activity of plasma lecithin: cholesterol acyltransferase was significantly increased by fenofibrate and probucol. Analysis of the correlations between serum lipids and plasma lipolytic enzymes suggests that the mechanism of the hypolipidaemic action of clofibrate and bezafibrate might be related to increased catabolism of triglyceride-rich particles; that of fenofibrate and probucol was less clear and might be multifactorial in origin.

Adult↗
PubMed1991

Effects of bezafibrate on hepatic cholesterol metabolism.

The influence of bezafibrate treatment on hepatic cholesterol metabolism was studied in rats and in humans. The activities of the three key enzymes involved in cholesterol metabolism [3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, cholesterol 7 alpha-hydroxylase, and acyl-coenzyme A: cholesterol acyltransferase (ACAT)] were suppressed by bezafibrate treatment in rats, but only the ACAT activity was significantly decreased when the activity was related to total liver weight. In humans, HMG-CoA reductase activity was increased about twice in the treated normolipidemic gallstone patients. In contrast, the concentration of lathosterol in serum decreased, indicating depression of the cholesterol synthesis. The increase in HMG-CoA reductase activity may be a compensatory effect of an inhibition of some other enzymes in the synthesis of cholesterol, as in vitro study on liver microsomes excluded a direct inhibitory effect of bezafibrate on HMG-CoA reductase. The ACAT activity was not significantly changed, and the cholesterol 7 alpha-hydroxylase activity was decreased by 55-60% compared with controls. The LDL-receptor-binding activity was unaffected by bezafibrate treatment.

Animals↗
PubMed1984

[Bezafibrate-induced myolysis and myoglobinuria in patients with impaired renal function].

A muscular syndrome has been described in patients on clofibrate and fenofibrate therapy. The present paper describes four patients with impaired renal function in whom symptoms and signs of skeletal muscle damage developed during treatment with another clofibrinic acid derivative, bezafibrate. The syndrome was characterized by variable degrees of muscular cramps and paresis, excessive elevation of muscle enzymes in serum, myoglobinemia and myoglobinuria. Transient deterioration of renal function was also common. All patients had been overdosed with bezafibrate with regard to their renal function. It is concluded that bezafibrate like other lipid lowering agents of the clofibrate type may induce muscle damage, at least if doses are not adjusted to renal function. Extreme caution is warranted when treating patients with renal impairment with bezafibrate and strict dose adjustment to kidney function is necessary to avoid muscle damage.

Aged↗
PubMed1988

Steady-state kinetics of bezafibrate retard in hyperlipidemic geriatric patients.

The pharmacokinetics of a slow-release formulation of bezafibrate were investigated under steady-state conditions in 19 hyperlipidemic patients between the age of 61 and 87 years and compared to the kinetics in 20 healthy volunteers (age 19-42 years). Maximum serum levels were 1.6-fold higher in the elderly, which was partly due to a diminished renal clearance caused by the reduction in renal function (CLCR 23-81 ml/min) and partly due to a decrease in extrarenal clearance (probably hydroxylation and hydrolysis). Evidence for the additional decrease in extrarenal clearance was provided by the greater decline in total drug clearance than would be anticipated from a mere reduction in glomerular filtration. Thus, dose adjustment of slow-release bezafibrate in elderly patients cannot be based merely on creatinine clearance. In general, it is recommended that bezafibrate retard is substituted by a reduced dose of normal-release bezafibrate below a creatinine clearance of 60 ml/min.

Administration, Oral↗
PubMed1994

Efficacy and safety of a combination fluvastatin-bezafibrate treatment for familial hypercholesterolemia: comparative analysis with a fluvastatin-cholestyramine combination.

PURPOSE: Familial hypercholesterolemia (FH) carries a markedly increased risk for coronary artery disease (CAD). Reduction of plasma low-density lipoprotein cholesterol (LDL-C) levels to the normal range may prevent premature atherosclerosis and usually requires a combination of cholesterol-lowering drugs. The major objective of this study is to compare two different drug combinations for the treatment of heterozygous FH. PATIENTS AND METHODS: The current investigation is a short-term, double-blind study comparing the efficacy and safety of fluvastatin when combined with cholestyramine (group 1) or with bezafibrate (group 2) in 38 patients with heterozygous FH. RESULTS: After 6 weeks of combination treatment, in comparison to a drug-free baseline (patients receiving single-blind placebo during the lead-in period of an earlier study, ie, before ever receiving fluvastatin), the combination of 40 mg/d of fluvastatin with 400 mg/d of bezafibrate in group 2 reduced plasma LDL-C levels by 35% as compared with 32% in group 1, and reduced the LDL-C/high-density cholesterol (HDL-C) ratio by 46%, compared to 37% in group 1 (a non-significant difference for both comparisons). When compared to an intermittent 6-week open-label administration of 40 mg fluvastatin monotherapy, the addition of cholestyramine or bezafibrate each reduced LDL-C by an additional 13% (P < 0.01 for both regimens). CONCLUSIONS: Fluvastatin-bezafibrate is superior to a fluvastatin-cholestyramine combination for lowering serum triglycerides and elevating HDL-C serum levels in patients in conjunction with a significant lowering of LDL-C/HDL-C ratios, and may be an effective synergistic therapy for heterozygous FH. No episodes of myositis were seen in this short-term study, a finding that is in agreement with most of the reported studies on statin-fibrate combinations reviewed here.

Adult↗
PubMed1982

Treatment of familial hypercholesterolemia with a combination of bezafibrate and guar.

The effect of guar (15.6 g/day), a dietary fibre, and simultaneous administration of bezafibrate (600 mg/day) during dietetic treatment on the plasma lipoproteins and apolipoproteins was investigated in 12 patients with familial hypercholesterolemia (corresponding to the HLP type IIa pattern). Either bezafibrate alone or bezafibrate in combination with guar was administered in a cross-over study for 3 months. Guar led to an additional lowering of the total cholesterol in the plasma by 7% (P less than or equal to 0.05) associated with a fall of the low density lipoprotein cholesterol (LDL-cholesterol (LDL-cholesterol) by 13% (P less than or equal to 0.01) without any changes in the very low density lipoprotein (VLDL) and high density lipoprotein (HDL) cholesterols. In parallel with the decrease in LDL-cholesterol, the apoprotein B also was diminished by 20% (P less than or equal to 0.05). The plasma triglyceride level and the triglyceride distribution within the individual lipoprotein fractions were not altered in any consistent manner by the addition of guar. Neither the fasting plasma glucose level nor the body weight were affected. The side-effects due to guar treatment consisted of slight nausea, meteorism and constipation, but this did not in any of the cases lead to early termination of the study. These results demonstrate that guar exerts its cholesterol-lowering effect in addition to that of bezafibrate.

Adult↗
PubMed1987

Effect of bezafibrate on lipoprotein secretion by cultured human hepatocytes.

The secretion of newly synthesized very low density lipoprotein and low density lipoprotein (VLDL + LDL) and high density lipoprotein (HDL) in cultured human hepatocytes in the presence or absence of bezafibrate added to the culture medium has been evaluated. The content of triacylglycerol, apolipoprotein B, 3H-labeled proteins and 14C-labeled lipids accumulated in a culture medium increased linearly for periods up to 18 h. During incubation, cellular triacylglycerol content was unchanged. This hypolipidemic agent, at a concentration of 10 microM, inhibited secretion of the several VLDL + LDL [3H]apolipoproteins and the VLDL + LDL [14C]lipids, suggesting it can affect the processes of biosynthesis and secretion. The secretion of total [3H]apolipoproteins in the HDL fraction and [3H]protein (d greater than 1.21 g/ml) was unchanged after an exposure to bezafibrate (10 microM). Incubation in the presence of 10 microM bezafibrate resulted also in decreases in both total VLDL neutral lipids and apolipoprotein B secreted into the medium. These results indicate that bezafibrate might exert its plasma lipid-lowering effect by suppressing the VLDL production in liver and reducing the secretion of VLDL into the circulation.

Bezafibrate↗
PubMed1987

Influence of bezafibrate and colestipol on LDL-cholesterol, LDL-apolipoprotein B and HDL-cholesterol in hyperlipoproteinaemia.

A significant increase of LDL-apolipoprotein B by 13% and LDL-cholesterol by 19% was observed in a group of 9 patients with hyperlipoproteinaemia Type III after bezafibrate treatment. Additional administration of colestipol caused a significant decrease of both LDL-apolipoprotein B by 18% and LDL-cholesterol by 25%. In 10 patients of hyperlipoproteinaemia Type IIb a significant decrease of both LDL-apolipoprotein B by 28% and LDL-apolipoprotein B by 18% was observed after bezafibrate therapy. When bezafibrate was given together with colestipol a further decrease of both LDL-cholesterol by 17% and LDL-apolipoprotein B by 16% occurred. HDL-cholesterol concentration increased significantly in both groups of hyperlipaemic patients during therapy. This may be the effect of both bezafibrate and colestipol. It is concluded that bile acid resins may effectively prevent the LDL-cholesterol concentration increase observed sometimes after clofibrate analogues.

Adult↗
PubMed1987

High density lipoprotein alterations induced by bezafibrate in healthy male volunteers.

The alterations of HDL structure and metabolism induced by bezafibrate administration were studied in healthy male volunteers. As usually observed in hyperlipaemic patients, bezafibrate induced a decrease of the plasma concentrations of apo B and LDL-cholesterol and an increase of that of HDL-cholesterol. Analysis of HDL by gradient polyacrylamide gel electrophoresis revealed that bezafibrate administration resulted in a change of the particle size distribution likely suggesting a drop of the HDL2/HDL3 ratio. This was accompanied by a 30% enhancement of the plasma concentration of apoprotein A-II, while that of apoprotein A-I remained unchanged. These data suggest an increase of the HDL concentration, preferentially in the HDL3 subfraction. In spite of these HDL alterations, there was no evidence of change in the three stages of the reverse pathway of cholesterol, since bezafibrate did not induce any significant alteration in the in vitro properties of plasma with respect to (a) cholesterol transport from cultured cells, (b) cholesterol esterification, and (c) transfer of cholesteryl esters from HDL to VLDL-LDL.

Adult↗
PubMed1990

Interruption of long-term lipid-lowering treatment with bezafibrate in hypertriglyceridaemic patients. Effects on lipoprotein composition, lipase activities and the plasma lipid fatty acid spectrum.

When bezafibrate therapy was interrupted in patients who had been on continuous treatment for hyperlipoproteinemia for 4-10 years, there were significant increases in the serum cholesterol, triglyceride and apolipoprotein B concentrations corresponding to an increase of the very low density lipoprotein (VLDL) levels by approximately 50%. This increase of VLDL was accompanied by reduced levels of the post-heparin lipoprotein lipase activity (LPLA) (P = 0.07) and hepatic lipase (P = 0.05) activity with a significant reduction of the skeletal muscle LPLA (P less than 0.05), but not the adipose tissue LPLA, and a retarded removal of an i v injected fat emulsion (P less than 0.01). There were no significant changes of the low or high density lipoprotein cholesterol or the apolipoprotein A-I or A-II concentrations. Three months after bezafibrate treatment the content of linoleic and gammalinoleic acid in the plasma cholesterol ester had increased significantly, while the palmitoleic and oleic acids were reduced in spite of unchanged dietary treatment. Taken together, the data indicate that a lipid-lowering effect of bezafibrate, particularly on the VLDL lipids, is maintained throughout long treatment periods. One mechanism for the reduced level of the triglyceride-rich lipoproteins is an increased activity of the lipoprotein-lipase activity in the skeletal muscle, which decreased when the treatment was interrupted. The significance of the changes of the plasma lipid fatty acid spectrum during bezafibrate treatment remains unclear.

Aged↗
PubMed1992

The effect of bezafibrate on very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), and low density lipoprotein (LDL) composition in type 1 diabetes associated with hypercholesterolaemia or combined hyperlipidaemia.

Lipoprotein composition was examined in type 1 diabetic subjects with hypercholesterolaemia +/- hypertriglyceridaemia during a 3-month double-blind placebo controlled assessment of bezafibrate therapy. The predominant effect was on lipoprotein lipid content. In those with hypercholesterolaemia alone, bezafibrate significantly reduced the cholesterol (particularly esterified cholesterol) and triglyceride content of large very low density lipoprotein (VLDL) (Svedberg flotation units (Sf) 60-400) in comparison to the placebo group (P less than 0.05), and a trend towards a reduction in free and esterified cholesterol within the intermediate density lipoprotein fraction (IDL) (Sf 12-20) was noted. Low density lipoprotein (LDL) composition was unaltered and in general phospholipid and protein concentrations and cholesteryl ester/protein ratios within the lipoprotein fractions were unaffected. Large VLDL cholesterol and triglyceride concentrations in those with combined hyperlipidaemia were significantly decreased following bezafibrate therapy, both in comparison to placebo-treated subjects and to baseline concentrations (P less than 0.05). An additional significant reduction in small VLDL (Sf 20-60) free cholesterol was recorded (P less than 0.05). Average reductions of large and small VLDL protein of 50-56% were not significant because of wide variation in responses. Bezafibrate had no effect on the abnormal composition of IDL and LDL, characteristic of Type 1 diabetes, regardless of whether or not hypertriglyceridaemia was associated with hypercholesterolaemia. Its major action was to lower VLDL lipid concentrations, but it may also reduce the lipid content of intermediate density lipoprotein in Type 1 diabetes.

Adolescent↗
PubMed1988

Hypertriglyceridemia and hyperuricemia: effects of two fibric acid derivatives (bezafibrate and fenofibrate) in a double-blind, placebo-controlled trial.

The effects of bezafibrate and fenofibrate on serum lipoproteins and serum urinary uric acid were compared. In a double-blind, placebo-controlled, cross-over study, each drug was administered in random order for 6 weeks followed by a 3-week drug-free phase to ten men with primary hypertriglyceridemia. Serum triglyceride and cholesterol concentrations decreased significantly with both fenofibrate and bezafibrate, although no significant change in serum apolipoprotein B, serum low density lipoprotein (LDL) cholesterol or serum high density lipoprotein (HDL) cholesterol concentrations was apparent. Serum uric acid levels, which were elevated on placebo and bezafibrate, were significantly reduced by 20% by fenofibrate. This was associated with an increase in renal uric acid clearance of 30% during fenofibrate therapy. Because it seems likely that hypertriglyceridemia and hyperuricemia are linked by a common carbohydrate inducibility, we studied the acute hyperuricemic response to orally administered fructose. Fructose (50 g) caused the anticipated rise in serum urate reaching a peak between 60 and 90 minutes, which was quantitatively greater in the men with hypertriglyceridemia than in healthy controls. The serum uric response to fructose was unaffected by bezafibrate, but was converted to normal by fenofibrate. The hyperuricemic action of fenofibrate is of sufficient magnitude to be of therapeutic value in the management of patients whose hypertriglyceridemia is associated with gout.

Bezafibrate↗